Reports
Fat-specific Protein 27 Inhibits Lipolysis by Facilitating the Inhibitory Effect of Transcription Factor Egr1 on Transcription of Adipose Triglyceride Lipase*

https://doi.org/10.1074/jbc.C114.563080Get rights and content
Under a Creative Commons license
open access

Lipolysis in fat tissue represents a major source of circulating fatty acids. Previously, we have found that lipolysis in adipocytes is controlled by early growth response transcription factor Egr1 that directly inhibits transcription of adipose triglyceride lipase, ATGL (Chakrabarti, P., Kim, J. Y., Singh, M., Shin, Y. K., Kim, J., Kumbrink, J., Wu, Y., Lee, M. J., Kirsch, K. H., Fried, S. K., and Kandror, K. V. (2013) Mol. Cell. Biol. 33, 3659–3666). Here we demonstrate that knockdown of the lipid droplet protein FSP27 (a.k.a. CIDEC) in human adipocytes increases expression of ATGL at the level of transcription, whereas overexpression of FSP27 has the opposite effect. FSP27 suppresses the activity of the ATGL promoter in vitro, and the proximal Egr1 binding site is responsible for this effect. FSP27 co-immunoprecipitates with Egr1 and increases its association with and inhibition of the ATGL promoter. Knockdown of Egr1 attenuates the inhibitory effect of FSP27. These results provide a new model of transcriptional regulation of ATGL.

Adipocyte
Adipose Triglyceride Lipase (ATGL)
Early Growth Response Protein 1 (EGR1)
Lipid Droplets
Lipolysis

Cited by (0)

*

This work was supported by Grants DK52057 and AG039612 from the National Institutes of Health, Grant 7-11-BS-76 from the American Diabetes Association, and a research award from the Allen Foundation (to K. V. K.); National Institutes of Health Grants R56DK094815 and 8KL2TR000158 (from the parent grant UL1-TR000157 to the Clinical and Translational Science Institute, Boston University); and Boston Nutrition and Obesity Research Center Pilot Grant P30DK046200 (to V. P.).

This article contains supplemental Figs. S1 and S2.